α-MSH C-terminal tripeptide (research anti-inflammatory)
KPV
Lys-Pro-Val fragment of α-MSH studied for -independent and MC1R-related anti-inflammatory effects in gut and skin models.
Primary Mechanism of Action
Clinical / Scientific
KPV is the C-terminal tripeptide of α-melanocyte-stimulating hormone. Experimental work suggests anti-inflammatory activity, including PepT1-mediated uptake in intestinal epithelium and suppression of NF-κB-related signalling in models. Not an approved IBD drug.
Pathway Targets
NF-κB
Scientific explanation
Reported suppression in epithelial models.
MC1R / melanocortin signalling
Scientific explanation
Possible contribution; some KPV effects may be -independent.
Pathway Convergence
Clinical / Scientific
Target → pathway → downstream effect → biological consequence. This is a mechanistic map, not a treatment claim.
Receptor to physiology
Target to downstream effect: NF-κB → MC1R / melanocortin signalling
Mechanistically Relevant Repurposed & Adjunctive Applications
Research peptide context
PreclinicalMechanistic rationale
Catalogued as a research peptide. Mechanistic statements below describe known or pathway biology and do not establish a licensed therapeutic indication.
Mechanistic Application Matrix
| Biological Target | Mechanism | Potential Relevance | Evidence Level |
|---|---|---|---|
| NF-κB | Experimental suppression | Epithelial inflammation models | Preclinical |
In Plain Language
KPV is a three-amino-acid tail of a pigmentation hormone, studied for calming inflammatory switches in gut and skin cells in the lab.
Mechanistic information is provided for scientific and educational purposes. Discussion of biological pathways or investigational applications does not establish clinical efficacy or constitute individualized medical advice.